Polio,
or more properly poliomyelitis, was one of the most feared and studied
diseases of the first half of the 20th Century. Though the Salk and later
the Sabin vaccines have essentially eliminated the disease in developed
countries, many mysteries regarding polio remain. This is probably due
to the fact that as polio epidemics ended in North America and Europe,
research on the disease also came to an abrupt halt. Thus, as LaForce (1983)
noted, knowledge about the epidemiology and pathology of polio is essentially
frozen at a mid-1950s level.

In the paragraphs
that follow, I will define the disease of polio and explore some of the
mysteries that still surround it. Other sections of this site document
polio's history, describe its late effects, and provide excerpts from narrative
accounts of various aspects of the polio experience.

Poliomyelitis
is an "inflammation of the gray matter of the spinal cord (Taber, 1970,
p. P-77). Though the word "poliomyelitis" sounds complicated and impressive,
it was formed by putting together the Greek words for the site of the disease
- polios, meaning gray,myelos, meaning marrow,
and adding the English suffix, itis, meaning inflammation.
It has gone by many names including infantile paralysis, Heine-Medin's
Disease, debility of the lower extremities, and spinal paralytic paralysis.
In common usage, the term poliomyelitis is abbreviated to polio.

Polio is caused
by a virus which results in an acute infection. However, contrary
to what is commonly believed, the virus did not typically result
in paralysis. Rather, the majority of infected individuals experienced
only mild respiratory or gastrointestinal symptoms, often accompanied by
fever, headache, and muscle stiffness. These symptoms lasted only a few
days, and many had such mild cases that they did not even realize they
were ill. Therefore, they often continued on with there daily routines,
attending school or work, and exposing many others to the polio virus.
This fact helps explain the reports of many polio survivors that they were
the
only ones in their family, neighborhood, or community to have had polio.
In actuality, there could have been many individuals with whom they came
into contact who had theminor illness, as non-paralytic
polio was often called.

Only in a small
number of cases did the virus penetrate the central nervous system, causing
the major illness, or "true polio." In these cases, neurons (nerve
cells) in the anterior horns of the spinal cord and the lower brain were
affected, resulting in "tightness in the neck, back, and hamstring muscles
as well as varying degrees of muscle weakness, as paralysis sets in" (Owen,
1990, p. 211). Though there was never a cure for polio, most who contracted
it experienced improvement in muscle strength and control after the acute
infection subsided. In some cases, however, motor neurons were left severely
damaged or completely destroyed, resulting in permanent weakness or paralysis,
most commonly to the lower extremities (Headley, 1995).

There are actually
three separate strains or immunologic types of the disease: Type I (Brunhide),
Type II (Lansing), and Type III (Leon). Most epidemics, at least
in the United States, were the result of Type I virus (Nathanson and Martin,
1979).

The means by which
the polio virus enters the central nervous system is still not definitely
known. (Taber, 1970). However, it is interesting to note that relatively
recent data from third-world nations suggests that when those experiencing
acute polio are given injections such as DPT immunizations, antibiotics,
antimalarials, or antipyretics, the injected limb develops paralysis within
one week (LaForce, 1983).

Though this connection
between injections and paralysis has repeatedly been demonstrated, "the
mechanism by which this phenomenon occurs is not well understood. (However)
the best evidence to date suggests the trauma initiates a reflex dilation
of blood vessels at the corresponding spinal cord level and facilitates
entry of the virus" (LaForce, 1983, p. 30).

Other factors
thought to predispose individuals to the major disease were pregnancy and
tonsillectomy, as well as other nose and throat procedures. Why these conditions
were likely to increase the risk of the disease entering the central nervous
system remains unknown.

There is also
still some mystery surrounding the exact means by which the polio virus
is transmitted. As Smith (1990) noted in her history of the development
of the Salk vaccine, "Nobody has ever completely settled the question of
how polio is spread, though the best evidence suggests the virus is excreted
in the stool and passed through hand-to-hand contact . . ." (p. 36).

The belief that
the polio virus is spread by contact with the feces of an already infected
person has been offered as an explanation for the increased incidence of
polio in developed countries such as the United States during the 20th
Century. According to this theory, before the advent of modern sewage treatment
plants and other improvements in public sanitation, virtually all individuals
were exposed to the polio virus early in their lives when they were at
least partially protected by maternal antibodies. Thus, they developed
mild, non-paralytic infections, probably during infancy, which provided
them with lifelong immunity. However, with better sanitation, both these
early infections as well as the likelihood of receiving antibody protection
decreased, resulting in greater susceptibility to paralytic polio. Thus,
in the words of Smith:

Put simply,
paralytic polio was an inadvertent by-product of modern sanitary conditions.
When people were no longer in contact with the open sewers and privies
that had once exposed them to the polio virus in very early infancy when
paralysis rarely occurs, the disease changed from an endemic condition
so mild that no one knew of its existence to a seemingly new epidemic threat
of mysterious origins and terrifyingly unknown scope (p. 23).

This central theory
regarding the spread of polio is supported, at least to some extent, by
experiences in third world countries. During World War II, for instance,
U.S. and British troops stationed in undeveloped countries were much more
likely to contract polio than native peoples, who apparently had already
developed immunity (Paul, 1971). Even in the 1970's, when individuals
from developed countries came into contact with those from a country without
a modern sanitation system, the incidence of paralytic polio was about
twenty times greater for those from the developed country (Nathanson and
Martin, 1979).

The above explanation for the transmission of polio is generally accepted
and seems quite logical. However, the incidence of the disease in
the United States during the epidemic years was very irregular, not only
from year to year, but from area to area, apparently showing no relation
to improvements in sewage treatment. The actual reason for this variation
remains another of the polio mysteries. However, it has been suggested
that this variability was possibly due to increased virulence of certain
virus strains or the presence of environmental conditions that enhanced
the disease's transmission (Nathanson and Martin, 1979).

Regarding the second factor of environmental conditions, it is well documented
that polio was primarily a disease of the summer months. Readers
old enough to recall the epidemic years of the 1940's and 50's probably
have vivid recollections of community swimming pools and other public areas
being closed during the "dog days" of July and August. Perhaps this
was an appropriate precaution. The disease occurred thirty-five times
more frequently in August than in April (the month of lowest incidence).
Though no one really knows why this was the case, it does not appear that
seasonal variation in interpersonal contacts is a sufficient explanation.
Rather, it is more likely that warm, moist weather favored transmission
of the disease, as Bradshaw (1989) and others have noted. This is,
however, just a hypothesis. The actual reason for the seemingly random
appearance of polio epidemics remains a mystery to this day.